ABSTRACT:The transport properties of oxygen and water vapor through EVOH films as functions of relative humidity (RH) and temperature were studied. The results of oxygen and water vapor permeation demonstrated that temperature and RH markedly affected barrier properties of these films. In general, the EVOH films had minimal oxygen and water vapor permeabilities at a low RH, attributed to the reduced mobility of the polymer resulting from strong interactions between small water molecules and the polymeric matrix at low RH. Beyond 75% RH, the permeabilities increased considerably. In addition, the barrier performance of the EVOH films was found to be dependent on their ethylene content and orientation. From the experimental data, semiempirical equations describing oxygen transmission rates (O 2 TR) as functions of RH and temperature were developed.

No abstract

Moisture sorption kinetics of nonoriented ethylene vinyl alcohol copolymer (EVOH) film (EF‐E15) were studied at 25, 35, and 45°C. Anomalous diffusion was observed for the polymeric film at high relative humidities (RH) and higher temperatures. Diffusion and solubility coefficients of water were found to be concentration dependent. The moisture sorption isotherms of three types of EVOH films (EF‐E15, EF‐F15, and EF‐XL15) determined at 25, 35, and 45°C, were well described using the GAB equation. Glass transition temperatures (Tg) of the EVOH films, as influenced by RH, were measured using differential scanning calorimetry. Tg values decreased with increasing RH due to the plasticization effect of water, and were found to be dependent on ethylene content and orientation of the EVOH films. © 1999 John Wiley & Sons, Inc. J Polym Sci B: Polym Phys 37: 691–699, 1999

No abstract

BackgroundWe attempted to determine whether the inflammatory pathway HMGB1-TLR4 and the downstream pro-inflammatory cytokines is upregulated in focal cortical dysplasia (FCD) type II and whether there is a correlation between the TLR4 upregulation and disease duration or frequency of epileptic seizures.MethodsFCD type II and peri-FCD paired tissues resected from eight children with refractory epilepsy were collected. Through real-time qPCR, Western blot, and co-immunoprecipitation, we examined the differences between FCD lesions and peri-FCD tissues with respect to mRNA expression, protein expression, and protein interaction in HMGB1-TLR4 pathway biomarker and downstream pro-inflammatory factors in whole brain tissue. Then, we used immunofluorescence to examine the difference between FCD lesions and peri-FCD tissues with respect to protein expression and intracellular distribution of HMGB1-TLR4 pathway biomarker in neurons, astrocytes, and oligodendrocytes. Correlation between level of TLR4 expression and disease duration or frequency of epileptic seizures in patients was also analyzed.ResultsThe protein expression levels of TLR4, cytoplasm HMGB1, TLR4/MyD88 complex, ubiquitination of TRAF6, p-IKK, p-IκB-α, p-NF-κB p65, and IL-1β and TNF-α in lesion tissues were significantly higher than those in peri-FCD controls. Total mRNA expression levels of TLR4, IL-1β, and TNF-α in lesion tissues were significantly higher than those in peri-FCD controls, but HMGB1 had no significant change. In neurons and astrocytes inside the lesions, the expression of TLR4 protein was significantly higher than that in peri-FCD tissues, and HMGB1 was mainly expressed in the cytoplasm, while expressed in the nuclei in peri-FCD tissues. But in oligodendrocytes, there was no upregulation of HMGB1-TLR4 pathway in both lesions and peri-FCD tissues. We did not identify the correlation between the level of TLR4 activation and disease duration or frequency of epileptic seizures.ConclusionThe HMGB1-TLR4 pathway was upregulated in the neurons and astrocytes inside FCD type II lesions, which led to an increase in the release of downstream pro-inflammatory cytokines. Correlation between the level of TLR4 activation and duration or frequency of epileptic seizures was not identified.

No abstract

It is widely accepted that the cytotoxicity and genotoxicity of benzene results from the action of reactive metabolites. Therefore, genetic variation in metabolic enzyme genes may contribute to susceptibility to chronic benzene poisoning (CBP) in the exposed population. Using a case-control study that included 268 benzene-poisoned patients and 268 workers occupationally exposed to benzene in South China, we aimed to investigate the association between single-nucleotide polymorphisms in genes with phase I and II of metabolism and risk of CBP. The TaqMan technique was used to detect polymorphisms of CYP1A1, CYP1A2, CYP1B1, ADH1B, EPHX1, EPHX2, NQO1, MPO, GSTP1 and UGT1A6 genes. We also explored potential interactions of these polymorphisms with lifestyle factors such as cigarette smoking and alcohol consumption. A weak positive association was found between glutathione S-transferase pi-1 (GSTP1) rs1695 polymorphism and the risk of CBP (P = 0.046), but this association was not statistically significant (P = 0.117) after adjustment for potential confounders. Further analysis showed that the risk of CBP increased in the subjects with EPHX1 GGAC/GAGT diplotype (P = 0.00057) or AGAC/GAGT diplotype (P = 0.00086). In addition, we found that alcohol drinkers with the EPHX1 rs3738047 GA + AA genotypes and non-alcohol drinkers with the GSTP1 rs1695 AA genotype tended to be more susceptible to benzene toxicity. Our results suggest that genetic polymorphisms in EPHX1 may contribute to risk of CBP in a Chinese occupational population.

DNA damage induced by benzene is an important mechanism of its genotoxicity that leads to chronic benzene poisoning (CBP). Therefore, genetic variation in DNA repair genes may contribute to susceptibility to CBP in the exposed population. Because benzene-induced DNA damage includes single-and double-strand breaks, we hypothesized that single-nucleotide polymorphisms in X-ray repair crosscomplementing group 1 (XRCC1), apurinic/apyrimidinic endonuclease (APE1), ADP ribosyltransferase (ADPRT), X-ray repair cross-complementing group 2 (XRCC2), and X-ray repair cross-complementing group 3 (XRCC3) are associated with risk of CBP. We genotyped single-nucleotide polymorphisms at codons 194, 280, and 399 of XRCC1, codon 148 of APE1, codon 762 of ADPRT, codon 188 of XRCC2, and codon 241 of XRCC3 in 152 CBP patients and 152 healthy workers frequency matched on age and sex among those who were occupationally exposed to benzene. The genotypes were determined by PCR-RFLP technique with genomic DNA. We found that no individuals had the XRCC2 codon 188 variant alleles or Met/Met genotype of XRCC3 codon 241 in this study population. However, individuals carrying the XRCC1 194Trp allele (i.e., Arg/Trp+Trp/Trp genotypes) had a decreased risk of CBP [adjusted odds ratio (OR adj ), 0.60; 95% confidence interval (95% CI), 0.37-0.98; P = 0.041] compared with subjects with the Arg/Arg genotype whereas individuals carrying the XRCC1 280His allele (i.e., Arg/His+His/His genotypes) had an increased risk of CBP compared with those with the Arg/Arg genotype (OR adj , 1.91; 95% CI, 1.17-3.10; P = 0.009). The analysis of haplotypes of polymorphisms in XRCC1 showed that there was a 2.96-fold (OR, 2.96; 95% CI, 1.60-5.49; C 2 = 12.39, P = 0.001) increased risk of CBP for subjects with alleles of XRCC1 194Arg, XRCC1 280His, and XRCC1 399Arg compared with those carrying alleles of XRCC1 194Arg, XRCC1 280Arg, and XRCC1 399Arg. Therefore, our results suggest that polymorphisms at codons 194 and 280 of XRCC1 may contribute to CBP in a Chinese occupational population. (Cancer Epidemiol Biomarkers Prev 2005;14(11):2614 -9)